Remodelage bronchique dans l’asthme

Gras, Delphine; Bourdin, Arnaud; Chanez, Pascal; Vachier, Isabelle

doi:10.1051/medsci/20112711011

Cited by 12 publications

(4 citation statements)

References 35 publications

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“…Airway remodeling directly affects the outcome of asthma. It refers to the pathological changes of the airway, which include airway epithelial injury, epithelial fibrosis, hypertrophy, proliferation and migration of airway smooth muscle (ASM), an increased number of activated and muscle fibroblasts, goblet cell proliferation, mucus secretion, angiogenesis, decreased cartilage integrity and increased airway vascularity ( 19 ). Numerous types of inflammatory cell, including eosinophils, T lymphocytes, macrophages, mast cells and neutrophils, as well as airway structural cells, including ASM cells, epithelial cells and fibroblasts, release a variety of cytokines, including chemokines, growth factors and extracellular matrix protein.…”

Section: Discussionmentioning

confidence: 99%

Inflammation and airway remodeling of the lung in guinea pigs with allergic rhinitis

Chen

Zhou

et al. 2017

Experimental and Therapeutic Medicine

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Allergic rhinitis (AR) and asthma belong to the category of type I allergic diseases, whose pathological features are airway remodeling of the lung and allergic inflammation. The aim of the present study was to evaluate inflammation and remodeling of lung tissue in a guinea pig model of AR in order to confirm consistent pathological changes of upper and lower airways in AR. Male guinea pigs were randomly divided into an experimental and a control group (n=10 in each). The AR model was established by sensitization through intraperitoneal injection of ovalbumin for three weeks and bilateral nasal local excitation for twelve weeks. All tissues of nasal mucosa and lung were subjected to hematoxylin and eosin as well as toluidine blue staining, and characteristics of remodeling of lung tissue, including thickness of bronchial wall, epithelial mucosa and smooth muscle were histologically determined. Collagen deposition in lung tissue was observed by Masson's trichrome stain. Severe paroxysmal nose scratching action, frequent sneezing, visible outflow of secretion from the anterior naris and frequent nose friction were observed in the AR model group within 30 min after local excitation. The total symptom scores were significantly increased in the AR model group compared with those in the control group. Obvious inflammatory cell infiltration was observed in the AR model group. Compared with those in the control group, the numbers of eosinophils and mast cells in nasal mucosa and lung tissue were significantly increased. Obvious airway remodeling of the lung was observed in the AR model group. Compared with those in the control group, bronchial wall thickness, epithelial layer thickness and smooth muscle thickness in the airways were significantly increased in the AR model group. Increased collagen deposition was found in the AR model group compared with that in the control group. The results of the present study revealed that inflammation and airway remodeling of lungs arose in guinea pigs with AR, suggesting that pathological changes of upper and lower airways are consistent in this AR model.

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Section: Discussionmentioning

confidence: 99%

Inflammation and airway remodeling of the lung in guinea pigs with allergic rhinitis

Chen

Zhou

et al. 2017

Experimental and Therapeutic Medicine

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“…Previous studies have shown that there are some wound-healing events in asthmatic airways, which were characterized by mucosa epithelial apoptosis/erosion, goblet cell hyperplasia/hypertrophy, thickening of basement membrane, epithelial fibrosis, submucosal gland hyperplasia, mucus secretion, hyperplasia of smooth muscle hypertrophy, hyperplasia of blood vessels, etc. [ 11 12 ] Studies on the abnormal injury and repair of upper airway allergic diseases are relatively scarce. A previous study showed that abnormal epithelial cell phenotype (epithelial-mesenchymal transition [EMT], characterized by downregulation of E-cadherin and cytokeratin and upregulation of vimentin) exists in nasal mucosal tissue in patients with CRSwNP.…”

Section: O Ne /U Nited a mentioning

confidence: 99%

Potential Role of Interleukin-25/Interleukin-33/Thymic Stromal Lymphopoietin-Fibrocyte Axis in the Pathogenesis of Allergic Airway Diseases

Yao¹,

Liu²,

Wang

2018

Chinese Medical Journal

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Objective:Allergic airway diseases (AADs) are a group of heterogeneous disease mediated by T-helper type 2 (Th2) immune response and characterized with airway inflammation and remodeling, including allergic asthma, allergic rhinitis, and chronic rhinosinusitis with allergic background. This review aimed to discuss the abnormal epithelial-mesenchymal crosstalk in the pathogenesis of AADs.Data Sources:Articles referred in this review were collected from the database of PubMed published in English up to January 2018.Study Selection:We had done a literature search using the following terms “allergic airway disease OR asthma OR allergic rhinitis OR chronic sinusitis AND IL-25 OR IL-33 OR thymic stromal lymphopoietin OR fibrocyte”. Related original or review articles were included and carefully analyzed.Results:It is now believed that abnormal epithelial-mesenchymal crosstalk underlies the pathogenesis of AADs. However, the key regulatory factors and molecular events involved in this process still remain unclear. Epithelium-derived triple cytokines, including interleukin (IL)-25, IL-33, and thymic stromal lymphopoietin (TSLP), are shown to act on various target cells and promote the Th2 immune response. Circulating fibrocyte is an important mesenchymal cell that can mediate tissue remodeling. We previously found that IL-25-circulating fibrocyte axis was significantly upregulated in patients with asthma, which may greatly contribute to asthmatic airway inflammation and remodeling.Conclusions:In view of the redundancy of cytokines and “united airway” theory, we propose a new concept that IL-25/IL-33/TSLP-fibrocyte axis may play a vital role in the abnormal epithelial-mesenchymal crosstalk in some endotypes of AADs. This novel idea will guide potential new intervention schema for the common treatment of AADs sharing common pathogenesis in the future.

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“…Asthma is a chronic bronchial inflammatory disease associated with several processes, including hyper-reactivity of the bronchi and local inflammation/thickening of the bronchial walls leading to mucus formation and bronchoconstriction. 1 2 3 According to the World Health Organization (WHO) estimates, nearly 235 million individuals suffer from asthma worldwide and its incidence, constantly increasing, is often underrated due to misdiagnosis. Though some cases of asthma, especially developing in childhood period, can be remitted and disappear, the disease is not usually curable for life because about 10% of asthma patients do not respond to currently available therapies 4 Asthma control is based on a daily background treatment (anti-inflammatory drugs, inhaled corticosteroids, or anti-leukotrienes) and an emergency treatment (fast-acting bronchodilators).…”

Section: Introductionmentioning

confidence: 99%

Overexpression of miR-155-5p Inhibits the Proliferation and Migration of IL-13-Induced Human Bronchial Smooth Muscle Cells by Suppressing TGF-β-Activated Kinase 1/MAP3K7-Binding Protein 2

Shi

Cao

et al. 2018

Allergy Asthma Immunol Res

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PurposeMolecular mechanisms leading to asthma is still ill-defined. Though the function of microRNAs (miRNAs) in asthma was previously reported, the involvement of miR-155 in important features of this disease remains unknown. The present study was designed to uncover the probable involvement of miR-155-5p in the proliferation and migration of IL-13-induced human bronchial smooth muscle cells (BSMCs) and the intrinsic regulatory mechanism.MethodsThe effects of different concentrations of IL-13 on the proliferation and migration of BSMCs as well as the expression of miR-155-5p and its predicted target transforming growth factor (TGF)-β-activated kinase 1/MAP3K7-binding protein 2 (TAB2) were investigated. The effects of miR-155-5p on the proliferation and migration of interleukin (IL)-13-induced BSMCs was determined in vitro using BSMCs transfected with miR-155 mimic/inhibitor and induced by a high concentration of IL-13. The quantitative real-time polymerase chain reaction (qRTPCR) was employed for determining the expression of miR-155-5p and TAB2. Western blotting was applied to analyze the expression of TAB2 at the protein level. Cell proliferation and migration were assessed using the 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) and Transwell assays, respectively.ResultsThe proliferation and migration of BSMCs were dose-dependently increased with IL-13 treatment. Contrariwise, IL-13 dose-dependently inhibited the expression of miR-155-5p in BSMCs. Mechanistic studies showed that inhibition of miR-155-5p further promoted the stimulatory effects of IL-13, whereas overexpression of miR-155 significantly inhibited these effects. In silico studies and luciferase reporter assays indicated that TAB2 was a negatively regulated miR-155-5p target.ConclusionsThese results suggested that miR-155-5p-inhibit the IL-13-induced proliferation and migration of BSMCs by targeting TAB2 and that the IL-13/miR-155/TAB2 pathway could serve as a therapeutic target for pulmonary diseases, especially asthma.

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Remodelage bronchique dans l’asthme

Cited by 12 publications

References 35 publications

Inflammation and airway remodeling of the lung in guinea pigs with allergic rhinitis

Inflammation and airway remodeling of the lung in guinea pigs with allergic rhinitis

Potential Role of Interleukin-25/Interleukin-33/Thymic Stromal Lymphopoietin-Fibrocyte Axis in the Pathogenesis of Allergic Airway Diseases

Overexpression of miR-155-5p Inhibits the Proliferation and Migration of IL-13-Induced Human Bronchial Smooth Muscle Cells by Suppressing TGF-β-Activated Kinase 1/MAP3K7-Binding Protein 2

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